Omega-3 polyunsaturated fatty acids and brain health: Preclinical evidence for the prevention of neurodegenerative diseases.
Trends in Food Science & Technology, online 20 Sept. 2017, https://doi.org/10.1016/j.tifs.2017.09.003
Olivier Kerdilesa, b, d, e, , Sophie Layéc, e, , Frédéric Calona, b, d, e, ,
Reminder: increasing Omega-3 increases by ~30% the amount of vitamin D which gets to cells
Omega-3 and Cognition (items in both categories)
- ADHD, Autism, Early Psychosis and Omega-3 – review Dec 2017
- Omega-3 found to treat Alzheimer’s and Parkinson’s in animals – Sept 2017
- Violent schizophrenia patients treated by 3 months of Omega-3 – RCT Aug 2017
- Psychosis risk reduced for 80 weeks by just 12 weeks of Omega-3 – RCT Aug 2017
- Alzheimer’s disease (apoE4) treatment may require multiple nutrients - May 2017
- Infants getting 1 g of Omega-3 for 12 weeks got better brains – RCT March 2017
- Omega-3 reduces many psychiatric disorders – 2 reviews 2016
- Cognitive Impairment 1.8 times more likely if low Omega-3– Oct 2016
- Omega-3 may treat schizophrenia
- Benefits of Omega-3 on brain development
- Omega-3 helps childhood cognition – meta-analysis April 2016
- Football Brain injuries prevented by Omega-3 – RCT Jan 2016
- Schizophrenia treated by 6 months of Omega-3 – RCT Nov 2015
- Omega-3 and infant development - dissertation Sept 2015
- Omega-3 etc improved both cognition and mobility of older women – Aug 2015
- Schizophrenia relapses reduced 3X by Omega-3 – RCT Mar 2015
- Cognitive decline in elderly slowed by Omega-3 – meta-analysis May 2015
- Cognitively impaired brain atrophy was slowed 40 percent by Omega-3 and B vitamins – RCT July 2015
- Omega-3, Vitamin D, and other nutrients decrease mental health problems – March 2015
- Vitamin D, Omega-3 supplementation helps cognition – perhaps due to serotonin – Feb 2015
- Vitamin D and Omega-3 may reduce cortical atrophy with age – Nov 2013
- Alzheimer’s and Vitamins D, B, C, E, as well as Omega-3, metals, etc. – June 2013
- TBI worse in rats if little Omega-3 in diet – June 2013
- Traumatic brain injury treated by Vitamin D Progesterone Omega-3 and glutamine – May 2013
Two tables summarizing rodent clinical trials
•Increasing brain DHA concentrations improves rodent performance in memory tests.
• Amyloid, tau, synaptic neuropathologies are improved by DHA in the most studies in animal models.
• N-3 PUFAs induce neuroprotection and partial neurorecovery in animal models of PD.
• N-3 PUFAs may act through neuroinflammatory pathways.
• Specific formulations of N-3 PUFAs from different sources can improve conservation and bioavailability.
As the prevalence of neurodegenerative diseases increases steadily, the need to develop new treatment approaches intensifies and the possibility of targeting risk and protective factors to delay onset of these diseases is attracting more interest. Dietary habits stand as one of the most promising modifiable risk factors for both Alzheimer's (AD) and Parkinson's (PD) diseases.
Scope and approach
Over the last 30 years, several groups have generated data indicating that concentrations of specific brain lipids highly depend on dietary intake. Preclinical results show that treatments with omega-3 polyunsaturated fatty acids (n-3 PUFA) improve cognition, provide neuroprotection (and even neurorestoration), reduce neuroinflammation and influence neuronal function, while high-fat diets exert deleterious effects. Preclinical experiments have been conducted in well-recognized animal models of AD, PD, and ischemic stroke.
Key findings and Conclusions
These studies have shown that dietary n-3 PUFA treatments consistently improve cognitive performance in animal models and may also exert disease-modifying actions. N-3 PUFA also provide protection to dopaminergic neurons in animal models of PD and possibly recovery after lesion. Furthermore, some of these effects might depend on specific diet formulations to protect long-chain fatty acids from oxidation or synergies with other nutrients. More generally, this review aims at providing evidence that adjustments in the consumption of dietary lipids alone or combined with other nutrients may be a cost-effective intervention to optimize brain function and prevent AD or PD.
Scientists, health professionals and the lay public increasingly recognize the potential benefit of nutrition in the prevention of CNS-related diseases. A steep rise in reported consumption of n-3 PUFA supplements was recently reported between 1999 and 2012 (Kantor, Rehm, Du, White, & Giovannucci, 2016). However, since the diagnosis of NDD is made a long time after disease onset, we may wonder if it is not too late to intervene. Manipulating dietary intake of fatty acids could be a relevant strategy to postpone the appearance of the more severe symptoms of NDD. Animal, epidemiology and non-AD clinical data all suggest cognitive benefits of n-3 PUFA, while animal studies may highlight evidence of disease modifications. Clinical evidence however remains limited to possible benefits in prodromal stages. It could also be interesting to combine n-3 PUFA with other nutrients such as polyphenols, which may also have cognitive benefits. Indeed, with the Neurophenols Consortium, our group has just reported the cognitive benefits of polyphenol extracts in the 3xTg-AD animal model of AD, without clear impact on canonical neuropathological markers (Dal-Pan et al., 2017).
It will still be difficult to adopt the best omega-3 PUFA supplementation strategy, as we need a better understanding of mechanisms of NDD. That includes pharmacodynamic and pharmacokinetic studies. A more precise knowledge of AD pathogenesis and PUFA metabolism could lead to the constitution of different subgroups of patients more likely to take benefit of omega-3 PUFA supplementation. Furthermore, larger clinical trials on prevention should be made in order to understand the real impact of omega-3 PUFA on neuroprotection in the population. In summary, literature shows that many nutrients (n-3 PUFA, polyphenols, antioxidants …) have a potential benefit in the prevention of diseases and especially those related to the CNS through direct effect on brain function and not necessarily related to classical pathophysiological cascades. As NDD prevalence will continue to rise in the next decades, prevention strategies based on nutrition needs to be thoroughly investigated now, in the hope of defining an optimal diet for the aging brain.